Remarkably, in conjunction with a 2-week sub-therapeutic course of RPM, deletion of HDAC11, or concomitant use of an HDAC11i in WT recipients, resulted in long-term cardiac allograft survival, as well as protection against the development of transplant arteriosclerosis, a hallmark of chronic allograft dysfunction and a common complication of clinical organ transplantation28. Here, HDAC11 is linked to arteriosclerosis disorder.